Viral infection during pregnancy correlates with increased frequency of neurodevelopmental disorders in offspring, a phenomenon well studied in mice prenatally subjected to maternal immune activation (MIA). Gloria Choi and her colleagues have previously shown that MIA-affected offspring display both cortical and behavioral abnormalities, whose induction depends on the T helper 17 (Th17) cell/interleukin-17a (IL-17a) pathway1,2. Choi recently obtained data showing that these cortical abnormalities are preferentially localized to a region encompassing the dysgranular zone of the primary somatosensory cortex (S1DZ) in mice and that these abnormalities are causal to the emergence of MIA-induced mouse behavioral phenotypes3. S1DZ has been shown to mainly respond to proprioceptive inputs, such as the movement of joints and stretch of muscle receptors.
In order to understand how the activity in this particular region of the primary somatosensory cortex is driving multiple ASD-like behaviors in these animals, it will be crucial to understand how the sensory information feeding into the S1DZ is differentially processed in the downstream neural circuits. Thus, Choi’s team proposes to anatomically and functionally delineate efferent targets of S1DZ in the MIA mouse model and assess their roles in eliciting MIA-induced behavioral abnormalities.